A 55-year-old man with known cirrhosis develops refractory ascites. His serum Na is 128 mEq/L, urine osmolality is 600 mOsm/kg, and urine Na is 8 mEq/L. The primary physio-pathological mechanism driving his hyponatraemia is:
- A Salt-wasting nephropathy from portal hypertension
- B Dilutional: baroreceptor-mediated non-osmotic ADH release ✓
- C SIADH secondary to hepatic encephalopathy
- D Hypothyroidism-induced ADH hypersecretion
Correct answer: B. Dilutional: baroreceptor-mediated non-osmotic ADH release
Explanation
In decompensated cirrhosis, decreased effective arterial blood volume activates baroreceptors which stimulate non-osmotic ADH secretion. ADH causes water retention disproportionate to solute, diluting serum Na. The high urine osmolality with very low urine Na (avid Na retention) confirms preserved aldosterone-driven Na reabsorption with excess free water retention — the hallmark of dilutional hyponatraemia in cirrhosis.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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